Abstract

Perinatal asphyxia (PA) is a major determinant of neurologic disability. In the immature brain, dopaminergic neurons are very sensitive to asphyxia, and abnormal dopamine levels can lead to functional and morphologic disturbances. The early dopaminergic input from the midbrain may play an important role in the development of the basal ganglia and the cerebral cortex.1 In newborn animal models, an excessive increase in extracellular dopamine is seen shortly following PA.2 But PA also produces long-lasting abnormalities in the dopaminergic pathways (mainly in the mesostriatal/mesolimbic dopamine system).2 Monoamine changes following PA have seldom been reported in human newborns and always restricted to the first hours of life, showing higher CSF dopamine metabolites in moderate-to-severe PA than in control or mild cases.3 Within the CNS, the end product of dopamine is homovanillic acid (HVA) and of serotonin, 5-hydroxyindoleacetic acid (HIAA); both can be measured in CSF. We describe chronological changes in cerebral monoamine neurotransmitters in newborns following a moderate to severe PA. ### Methods. We recruited seven term infants …

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